7 research outputs found

    Fully differential cross sections for photo-double-ionization of D2

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    We report the first kinematically complete study of the four-body fragmentation of the D2 molecule following absorption of a single photon. For equal energy sharing of the two electrons and a photon energy of 75.5 eV, we observed the relaxation of one of the selection rules valid for He photo-double-ionization and a strong dependence of the electron angular distribution on the orientation of the molecular axis. This effect is reproduced by a model in which a pair of photoionization amplitudes is introduced for the light polarization parallel and perpendicular to the molecular axis

    Complete Photo-Fragmentation of the Deuterium Molecule

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    All properties of molecules - from binding and excitation energies to their geometry - are determined by the highly correlated initial-state wavefunction of the electrons and nuclei. Details of these correlations can be revealed by studying the break-up of these systems into their constituents. The fragmentation might be initiated by the absorption of a single photon1-6, by collision with a charged particle7,8 or by exposure to a strong laser pulse9,10: if the interaction causing the excitation is sufficiently understood, the fragmentation process can then be used as a tool to investigate the bound initial state11,12. The interaction and resulting fragment motions therefore pose formidable challenges to quantum theory13,15. Here we report the coincident measurement of the momenta of both nuclei and both electrons from the single-plioton-induced fragmentation of the deuterium molecule. The results reveal that the correlated motion of the electrons is strongly dependent on the inter-nuclear separation in the molecular ground state at the instant of photon absorption

    Soluble IgM links apoptosis to complement activation in early alcoholic liver disease in mice

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    BACKGROUND: Ethanol feeding in mice activates complement via C1q binding to apoptotic cells in the liver; complement contributes to ethanol-induced inflammation and injury. Despite the critical role of C1q in ethanol-induced injury, the mechanism by which ethanol activates C1q remains poorly understood. Secretory IgM (sIgM), traditionally considered to act as an anti-microbial, also has critical housekeeping functions, facilitating clearance of apoptotic cells, at least in part through activation of C1q. Therefore, we hypothesized that 1) ethanol-induced apoptosis in the liver recruits sIgM, facilitating the activation of C1q and complement and 2) C1INH (C1 esterase inhibitor), which inhibits C1 functional activity, prevents complement activation and decreases ethanol-induced liver injury. METHODS: Female C57BL/6 wild-type, C1qa(−/−), BID(−/−) and sIgM(−/−) mice were fed ethanol containing liquid diets or pair-fed control diets. C1INH or vehicle was given via tail vein injection to ethanol- or pair-fed wild-type mice at 24 and 48 hours prior to euthanasia. RESULTS: Ethanol exposure increased aptoptosis in the liver, as well as the accumulation of IgM in the liver. In the early stages of ethanol feeding, C1q co-localized with IgM in the peri-sinusoidal space of the liver and accumulation of IgM and C3b was dependent on ethanol-induced BID-dependent apoptosis. sIgM(−/−) mice were protected from both ethanol-induced activation of complement and early ethanol-induced liver injury when compared to wild-type mice. Treatment with C1INH also decreased hepatic C3b deposition and ethanol-induced injury. CONCLUSION: These data indicate that sIgM contributes to activation of complement and ethanol-induced increases in inflammatory cytokine expression and hepatocyte injury in the early stages of ethanol-induced liver injury
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